One day post implant the chest X
One day post-implant, the chest X-ray showed the pacemaker lead in place within the RV (Fig. 1b, thick white arrow) with appropriate slack (thin black arrow). The pacemaker parameters were satisfactory and the patient was discharged home on the same day.
Two weeks after implantation, after returning from holidays, the patient presented with sudden onset of sharp chest pain associated with shortness of breath and palpitations. There was no evidence of deep vein thrombosis (DVT) or pulmonary embolism (PE). The ECG revealed complete atrio-ventricular block with atrial sense but intermittent loss of ventricular sense and capture (Fig. 1c).
The patient denied manipulation of or trauma over the pacemaker area. The chest X-ray showed that the ventricular lead had migrated below the lower hemi-diaphragm beyond the cardiac shadow, in closer proximity to the stomach (Fig. 1d, thick white arrow). The echocardiogram showed the lead penetrating through the RV apex myocardium, with a thin layer of anterior pericardial effusion (6mm) of no haemodynamic significance. Upon interrogation, complete loss of sense and capture was found at the ventricular lead.
Initial screening confirmed that the tip of the ventricular lead had perforated the RV and was in contact with diaphragm. Atrial lead appeared to go to reasonable position in RA. Under intravenous sedation and local anaesthesia, generator explanted and ventricular leads freed. Due to the absence of cardiac surgery on-site and the potential problems in transferring the patient to a tertiary cardiac centre, the decision was made to manage the patient conservatively, locally. The ventricular lead was pulled back to RV cavity and repositioned in RV with excellent acute parameters including normal lead impedance. Atrial lead was also repositioned with excellent acute parameters. Post-procedure echocardiogram confirmed no increase of the thin layer of pericardial effusion. The post-procedure course was uneventful. The patient was discharged home after 48h.
Discussion The common complications for most patients undergoing device TGF-beta Smad Compound Library are ecchymosis, haematoma at the incision site and chest discomfort, but these are usually short-lived. Major complications such as perforation of the major arteries or the heart itself, pneumothorax and sepsis can be fatal complications [1,6]. The clinical presentation of delayed cardiac perforation varies; dyspnoea, palpitations or chest pain due to pericardial effusion, haemothorax and extracardiac muscle stimulation can develop . Cardiac tamponade and death are very rarely associated with late myocardial perforations [7,8]. Myocardial perforations are divided into acute, subacute and delayed. Acute perforations occur within 24h of placement  and have an incidence of 1–7% [10–12]. Subacute perforations occur within 5–29 days of placement [9,10] and delayed perforations occur more than 30 days after placement . Subacute and delayed perforations are rare [5,10]. The rates of myocardial perforation are higher with active fixation leads [9,13–15], due to lead thickness and over-torquing [4,5,16]. Subacute and delayed perforations are thought to be increasing due to the increased flexibility of leads which cause increased force per unit of area on the ventricular wall  and this seems to be the likely cause in our described case. The clinical predictors of late cardiac perforation after pacemaker implantation include concomitant transvenous pacing, steroids within 7 days, older age, active fixation leads, Body Mass Index (BMI) <20, anticoagulation therapy and female gender [5,10,15,17,18]. The various complications of myocardial perforations can be present with a spectrum of symptoms from asymptomatic to sudden death . In cases of suspected lead perforation, device analysers, chest X-ray, ECG, echocardiography and fluoroscopy can be used to confirm the diagnosis . Normal impedance and pacing parameters do not exclude perforation . There has been decreased incidence of perforation when the lead is placed on the septal wall or in the right ventricular outflow tract where the ventricular wall is thicker as opposed to the right ventricular wall or the apex where the myocardium is thinner [5,9,13,16].